Visual System Flashcards
1
Q
Posterior INO of Lutz
A
2
Q
Categories of eye movement?
A
Conjugate
Vergence
3
Q
Types of conjugate eye movement
A
Horizontal:
Saccadic
Smooth pursuit
Vestibulo-ocular reflexes
Vertical:
Vertical
Smooth pursuit
4
Q
What is the purpose of conjugate eye movements?
A
To keep fovea of both eyes fixed on target object (fovea is at the centre of the macula) to maintain binocular vision
5
Q
What are vergence eye movements?
A
Axis of eyes do not move in parallel
6
Q
At what distance do vergence eye movements end?
A
>30m, beyond this the axes of the eyes are no longer parallel.
7
Q
What is common final pathway for conjugate horizontal eye movements
A
CN6 (interneuron) -> contralateral MLF -> CN3 (MR portion)
8
Q
Which nuclei are connected by MLF
A
3, 4, 6, 8, 11
9
Q
What is the cortical centre for horizontal saccadic eye movement?
A
Contralateral FEF (Frontal lobe)
10
Q
What is the pontine centre for saccadic eye movements
A
Ipsilateral PPRF
11
Q
Describe cortical generation of left saccadic horizontal conjugate gaze
A
Right FEF-> Descending fibres-> Left PPRF -> Abducens (motor)-> LR
+
Abducens (interneuron)- > right MLF to right CN3-> Right MR
12
Q
Where is the FEF found
A
Posterior middle frontal gyrus (in front of precentral gyrus)
13
Q
How do descending fibres from the FEF reach the PPRF
A
Either directly or via the ipsilateral superior colliculus
14
Q
Conjugate gaze palsy in FEF destruction
A
Towards affected size
15
Q
Conjugate gaze palsy in FEF activation (e.g. seizure)
A
Away from affected side
16
Q
Conjugate gaze palsy due to PPRF destruction
A
Away from affected side
17
Q
The manifestation of right MLF lesion?
A
When left eye abducts, the right eye will not adduct.
There is compensatory nystagmus of the left eye
INO
18
Q
Common causes of unilateral INO
A
Most common:
Demyelinating lesions e.g. MS.
CVA (e.g. brainstem infarction)
Trauma
Fourth ventricular tumours
SLE
Phenothiazine toxicity
19
Q
The manifestation of bilateral INO
A
Abduction of outer eye is preserved in both eyes but neither eye will adduct.
There will be nystagmus
20
Q
The most common cause of bilateral INO
A
Young: Inflammatory demyelinating condition
Old: Infarct or haemorrhage
Large tumours
Wernicke’s encephalopathy.
21
Q
What is the difference between internal, external and INO?
A
External ophthalmoplegia= EOM paralysis but pupil working
Internal opthalmoplegia= pupil not working but EOM working
INO= ophthalmoplegia due to internuclear lesions.
22
Q
How to differentiate between adduction palsy due to INO and adduction palsy due to damage to CN3 branch to medial rectus?
A
In INO adduction is preserved with convergence as pathways do not require MLF.
23
Q
Manifestation of left 1 and a half syndrome?
A
Loss of ipsilateral horizontal movement
Loss of contralateral adduction but not abduction
24
Q
Possible causes of 1 and a half syndrome?
A
Damage to ipsilateral PPRF and MLF
Or
Damage to ipsilateral, CNVI and MLF after it has crossed the midline from its site of origin.
25
The consequence of bilateral FEF damage?
Oculomotor apraxia
Nerves to EOM are intact, defect is in cortical saccadic generators bilaterally.
Preserved smooth tracking and VOR
https://collections.lib.utah.edu/ark:/87278/s64v2kqk
26
What structure within the semicircular canal detects rotational movements?
Collection of hair cells in the ampulla called the cristae. (cupula)
Endolymph moves towards the ampulla causing stimulation of the cupula
27
What is Scarpa's ganglion?
Afferent ganglion receiving fibres from the hair cells of the cupula of the semicircular canal
28
What is the main vestibular nucleus involved in VOR?
Medial vestibular nucleus
29
How is the medial vestibular nucleus connected with the contralateral abducens?
Via the MLF
30
With the leftward rotation of the head, what happens to the endolymph in either horizontal semicircular canal?
On the left endolymph is ampullopetal (i.e. towards the ampulla)
On the right endolymph is ampullofugal
31
What is the consequence of ampullofugal flow?
Endolymph moves away from kinocilium leading to inhibition
32
What happens to the VOR in an alert person on rightward rotation?
There is a slow conjugate horizontal movement towards the left, then right beat nystagmus due to cortical input - frontal lobe (corrective movement)
33
Why does warm water cause the eyes to deviate towards the contralateral side in the VOR?
Warm water causes expansion of endolymph, causing ampullopetal movement and stimulation of the kineocilia
In the conscious patient the fast phase of nytagmus will be towards the same side (COWS)
34
What happens when cold water is put into the right ear?
Eyes will deviate towards the same side, fast phase of nystagmus will be towards the contralateral side (COWS)
35
Explain COWS
In an alert patient during caloric testing.
Warm water into the right ear will cause eyes to deviate to the left, there will be fast phase nystagmus to the right (Warm same)
Cold water into the right ear will cause eyes to deviate to the right, there will be fast phase nystagmus to the left (Cold opposite)
36
Give reasons why optic nerve is not a nerve
Covered by oligodendrocytes
Affected by MS
Does not regenerate
Originates from diencephalon
Covered by meninges not epineurium
37
Describe the embryological development of the retina
Outpouching from neuroectoderm (optic vesicle)
Invaginated by the lens and becomes a double-layered optic cup
The outer part of the cup makes the choroid
Inner part makes the retina
38
Etymology of macula lutea?
Macula- spot
Lutea- yellow
39
Difference between macula lutea and fovea centralis?
Fovea contains maximal concentration of cones.
40
What is the differnece in the chemicals found in rods vs cones
Rods- Rhodopsin
Cones- iodopsin
41
Type of vision perceived by rods?
Scotopic
42
Type of vision perceived by cones?
Photopic
43
Which artery supplies the fovea?
Supplied by diffusion from the choroid, relatively avascular
44
What are the layers of the retina?
Pigment epithelial cells
Rod/Cone cells
Outer limiting membrane
Outer nuclear layer
Outer plexiform layer
Inner nuclear layer
Inner plexiform layer
Inner ganglion cells
Nerve fibre layer
Inner limiting membrane
45
From where do the first five (outer) layers of the retina derive their blood supply?
Diffusuion from choroid
46
Ganglion cells synapse where?
LGB
47
What is the most common site of retinal detachment?
Between pigmented epithelial layer and rod and cone layer
48
What is the destination of post-chiasmal fibres
Around 90% to ipsilateral LGN
Around 10% to the pretectal nucleus
49
How many layers of cells are there in the LGN?
6 layers
50
Into which layer of the LGN do ipsilateral (i.e. temporal retinal) optic tract fibres from the optic tract synapse?
2, 3, 5
Contralateral arrive in 1,4, 6
51
Which midbrain structure are involved in visual pathway?
Superior colliculus
Pretectal nucleus
CN3 motor nucleus
EW nucleus
52
Where do the 10% of optic tract fibres not reaching the LGN body synapse?
In the midbrain:
Superior colliculus
and
Pretectal nucleus
53
What is the name of the tract of fibres from the optic tract to the midbrain?
Superior brachium
54
Possible cause of bilateral nasal hemianopia?
Bilateral carotid artery masses
Calcification of the internal carotid arteries can impinge the uncrossed, lateral retinal fibers, leading to loss of vision in the nasal field.
55
Left homonoymous hemianopia
RAPD
Location of lesion
Optic tract (loss of fibres to pretectal nucleus)
56
Blood supply to the macula region of the occipital cortex?
PCA and MCA
57
Visual field deficit
BIlateral cuneal damage
Bilateral lower altitudinal hemianopia
58
Visual field defect
Bilateral lingual gyri destruction
Bilateral upper altitudinal hemianopia
59
Unilateral altitudinal hemianopia
Lesion location
Prechiasmal
60
Location of lesion
Monocoular visual loss with temporal upper quadrantopia
Optic nerve immediately adjacent to the chiasm.
61
Outline the pupillary light reflex
Light-\>Retina-\> optic nerve-\> chiasm-\> tract-\> superior bravchium)-\>pretectal nucleus (superior colliculus)-\> EW nucleus bilatearlly-\> CN3-\> Ciliary ganglion-\> pupillary constriction
62
What pathway connects both pretectal nuclei?
Posterior commissure
63
Which nerve carries postganglionic fibres from the ciliary ganglion?
Short ciliary nerve
64
What are the two portions of the EW nucleus
And the structures supplied
Rostral
Caudal
Rostral-\> constrictor pupillae
Caudal-\> ciliaris
65
Which part of the EW is stimulated by the pretectal nucleus?
Rostral
66
Which nucleus stimulates the caudal portion of EW and what pathway is it involved in?
Accommodation/Near response
67
Argyll-Robertson Pupil
ARP
Accommodation reflex preserved
Light reflex lost
Accommodates but does not react
68
Causes of Argyll-Robertson Pupil
Neurosyphilis
DM
SLE
69
Holmes Adie's pupil
Sluggish pupillary constriction
Does not constrict
70
Which type of receptor cells are found in the fovea centralis?
Cone cells which are responsible for colour vision
71
Cortical arrangement of projections from visual field
Inverted and reversed from right to left
72
Blood supply of optic nerve
Ophthalmic artery
73
Blood supply of optic chiasm
Superior:
Small perforators from ACA/AComm
Inferior:
Posterior circulation
Superior hypophyseal artery (ICA)
The central portion is exclusively supplied by the inferior netwok
74
Blood supply of optic tract
Anterior choroidal
75
Blood supply of LGN
Anterior and posterior choroidal arteries
76
Draw the light reflex
77
What are the components of the convergence reflex
Pupillary constriction
Ocular convergence
Thickening of lengs to accommodate near vision
78
Afferent limb of accommodation rfelx
Afferents to primary visual cortex
79
Efferent limb of accommodation reflex
Impulses originating in the visual association cortex, traversing the superior brachium and terminating in the pretectal area and superior colliculus
Superior colliculus stimulates CN3 MR portion and EW nucleus
80
Manifestation of optic nerve lesions
Complete- monocoular blindness
Partial- result in scotoma with central and then peripheral.
81
Why does an incomplete lesion of optic nerve result in scotoma
The papillomacular bundle conveying central vision is very vulnerable to extrinsic compression
Usually spreads from central to peripheral part of visual field rather than the other way round
82
Lesion location
Incomplete unilateral CN 2 lesion
83
Lesion location
Unilatearl complete prechiasmatic CN II lesion
84
def: Scotoma
Darkness
85
Possible manifestations of junctional lesions
Possible field defects:
Junctional scotoma of Traquair:
Monocular temporal field defect (pressure on crossing nasal fibres)
Monocular nasal field defect (pressure on crossing temporal fibres)
Junctional scotoma:
Monocular scotoma (pressure on optic nerve), contralateral superior temporal field defect (involvement of crossing nasal fibres)
86
Lesion location
Monocular temporal field defect
Junctional lesion
| (Junctional scotoma of Traquair)
87
Lesion location
Monocular nasal field defect
Junctional lateral lesion
Junctional scotoma of Traquair
88
Ipsilateral scotoma
Contralateral superior temporal field defect
Junctional scotoma
89
Lesion location
Junctional lesion
90
Anatomical basis of junctional scotoma
Lesions at the junction between the optic nerve and chiasm may damage both optic nerve fibres and fibres of Willebrand's knee (which are from inferonasal quadranat of optic nerve-\> superior temporal field defect)
Ipsilateral compresison on optic nerve results in central scotoma
91
Willebrand's Knee
Thought to be a loop of decussating fires that detours into contralateral optic nerve before entering optic tract
Carries inferior nasal quadrant fibres so damage results in contralateral superior temporal hemianopia
92
Is Willebrand's knee real?
Horton 1997 Trans Am Ophthal soc
Study in monkeys and humans involving injection of radioactive dye
Did not find decussating fibres detouring into ocontralateral optic nerve.
After monocular enucleation found that fibres were drawn into the entry zone of degenerating optic nerve
Not due to decussation but rather due to compression of optic chiasm and nerve atrophy
93
Anterior chiasmal syndrome
Junctional scotoma
Junctoinal scotoma of Traquair
94
Middle chiasmal lesion
Bitemporal hemianopia
95
Posterior chiasmal lesions
Smaller paracentral bitemporal field loss as macular fibres cross more posteriorly in the chiasm
Posterior lesions may also involve the optic tract and cause contralateral homonymous hemianopia.
96
Prefixed chiasm
Overlying the tuberculum sellae
97
Post-fixed chiasm
Overlying the dorsum sellae
98
Optic tract lesions
Incongruous homonymous hemianopia
99
What is the rule of congruity?
The more posterior the lesion in the retrogeniculate visual pathway, the more congruous the visual field defect
100
Why does the rule of congruity not apply to homonymous hemianopias?
As homonymous hemianopias are nonlocalising
101
Homonymous hemianopia localises to which portion of the visual field?
Retrochiasmal
102
A patient is having an anterior temporal lobectomy for the treatment of seizures. What is the anterior extent of Meyer’s loop in the temporal lobe?
A quantitative analysis of visual field defects related to anterior temporal lobectomy estimated an anterior extent of Meyer’s loop of 2.5 cm and a posterior extent of 7.5 cm with macular involvement at a resection length of 5.8 cm. Therefore, an anterior temporal lobectomy may produce some degree of a homonymous visual field defect when the resection is greater than 2.5 cm and a complete homonymous visual field defect when the resection is greater than 8 cm.
103
Which of the following may be seen with a homonymous hemianopia associated with a parietal lobe lesion?
Relative afferent pupillary defect
Macular sparing
Impairment of smooth pursuit towards the side of the lesion
Ipsilateral sensory changes
Impairment of smooth pursuit towards the side of the lesion
104
A right-handed patient is unable to read his own handwritten words. He also has a right homonymous visual field defect due to a stroke in the territory of the left posterior cerebral artery affecting the left occipital lobe. Which other structure is affected by the stroke?
Right angular gyrus
Splenium of the corpus callosum
Optic chiasm
Midbrain
Splenium of the corpus callosum
This patient has alexia without agraphia, which is a disconnection syndrome between the dominant angular gyrus (region of language processing in anterolateral parietal lobe) and the occipital lobe. Visual information is received by the right occipital lobe and is normally transferred to the left angular gyrus by the corpus callosum. This cannot occur if the splenium of the corpus callosum is damaged as in this case. The patient can write because the structures anterior to the splenium of the corpus callosum are intact, but cannot read these words.
105
What is the natural history of homonymous hemianopias?
Do not improve
Improve usually within the first 3 months and not after 6 months
Continuous improvement throughout life
Improvement up to 2 years after onset
A large natural history study of 263 homonymous hemianopias of various etiologies found that almost 40% improved. Improvement decreased with increasing time after injury. In most cases, improvement was within the first 3 months after injury and improvement after 6 months was mainly due to improvement in the patient’s ability to perform visual field testing reliably.
106
A patient presents with left hemianesthesia and hemiparesis and the following visual field defect. Where is the most likely location of the lesion?
Bilateral optic nerves
Optic chasm
Lateral geniculate nucleus
Occipital lobe
Lateral geniculate nucleus
Compressive and infiltrative lesions of the lateral geniculate nucleus (LGN) may cause an incongruous homonymous hemianopia. Vascular lesions may cause a “sectoranopia” due to the distinctive blood supply and retinotopic organization of the LGN (shown below). When sectoranopias occur, they are usually very congruous due to the well-defined vascular territories of the LGN. Involvement of neighbouring structures in the thalamus and pyramidal tracts may result in contralateral hemianesthesia or hemiparesis.
107
Homonymous horizontal sectoranopia
Posterior choroidal artery occ
108
Sector sparing homonymous hemianopia
Anterior choroidal artery occlusion
109
Meyer's loop injury results in
Contralateral superior quadrantopia
110
Complete colour blindness in presence of normal visual acuity suggests
Bilateral lesion in the inferiomedial temporooccipital lesion
111
Macular sparing inferior quadranopsia
Upper bank of calcarine sulcus
112
Macular sparing superior quadrantanopsia
Inferior bank of calcarine sulcus
113
Macular sparing homonymous hemianopia
Both banks of calacrine cortex sparing occipital pole
114
Incongruous hemianopia with RAPD
Pregeniculate retrochiasmal
115
Microsurgical anatomy of the sagittal stratum
Di Carlo et al
Acta Neurochirugica
116
What is this structure
Central retinal artery
117
In which direction should the superior ophthalmic vein be retracted when accessing the orbital apex?
Laterally, if retracted medially it can restrict access to the apex
118
https://www.neuroophthalmology.ca/textbook/disorders-of-eye-movements/v-prenuclear-disorders-brainstem/ii-internuclear-ophthalmoplegia-ino
